Transcranial modulation of brain oscillatory responses: A concurrent tDCS–MEG investigation

The physiological mechanisms underlying the effects of transcranial direct current stimulation (tDCS) are still largely unknown. To provide novel insight into the neurobiology of tDCS, stimulation was applied concurrently with Magnetoencephalography (MEG). This occurred while participants completed a visuomotor task before, during and after stimulation. Motor beta band (15–30 Hz) and visual gamma band (30–80 Hz) responses were localised using Synthetic Aperture Magnetometry (SAM). The resulting evoked and induced brain oscillatory responses were analysed. A significant reduction of average power was observed in the visual gamma band for anodal compared to sham stimulation. The magnitude of motor evoked responses was also demonstrated to be modulated by anodal tDCS. These results highlight that MEG can be used to draw inferences on the cortical mechanisms of DC stimulation

Stimulating somatosensory psychophysics: a double-blind, sham-controlled study of the neurobiological mechanisms of tDCS

In this study, the influence of tDCS on vibrotactile adaptation is investigated. Double-blind tDCS (Anodal/Sham) of 1 mA was delivered for 600 s to electrodes positioned in a somatosensory/contralateral orbit montage. Stimulation was applied between blocks of the implemented amplitude discrimination tasks. Amplitude discrimination thresholds were significantly degraded during adaptation trials, compared to those achieved at baseline but tDCS failed to modify task performance. Using Bayesian statistics, this finding was revealed to constitute substantial evidence for the null hypothesis. The failure of DC stimulation to alter performance is discussed in the context of several factors that may have confounded the induction of changes in cortical plasticity

Between Scylla and Charybdis: risks of early therapeutic anticoagulation for venous thromboembolism after acute intracranial hemorrhage.

OBJECTIVE: To assess the risk of hematoma expansion in patients with acute intracranial hemorrhage (ICH) requiring therapeutic anticoagulation for the treatment of venous thromboembolism. METHODS: We retrospectively reviewed all patients at our institution between 2014 and 2019 who were therapeutically anticoagulated for venous thromboembolism within 4 weeks after ICH. We included subtypes of traumatic ICH and spontaneous intraparenchymal hemorrhage. Our main outcome was the incidence of hematoma expansion within 14 days from initiating therapeutic anticoagulation. Hematoma expansion was defined as (1) radiographically proven expansion leading to cessation of therapeutic anticoagulation or (2) death due to hematoma expansion. Secondary outcomes included mortality due to hematoma expansion and characteristics associated with hematoma expansion. RESULTS: Fifty patients met inclusion criteria (mean age: 54 years, 80% male, 76% Caucasian); 24% had undergone a neurosurgical procedure prior to therapeutic anticoagulation. Median time from ICH to therapeutic anticoagulation initiation was 9.5 days (IQR 4-17), 40% received therapeutic anticoagulation in (12%) developed hematoma expansion, of whom two (4%) died. While not statistically significant, patients with hematoma expansion tended to be older (57.8 vs. 53.5 years), were anticoagulated sooner (4 vs. 10 days), presented with lower GCS (50% vs. 39% with GCS30 cc), and higher SDH diameter (16 mm vs. 8.35 mm). There was a trend towards greater risk of hematoma expansion for patients undergoing endoscopic ICH evacuation (16% vs. 2%, CONCLUSIONS: Our study is among the first to explore characteristics associated with hematoma expansion in patients undergoing therapeutic anticoagulation after acute ICH. Larger studies in different ICH subtypes are needed to identify determinants of hematoma expansion in this high-acuity population